“In the European Union, a disease is defined as rare when it affects fewer than 1 in 2,000 people.”

1 in 2000 people is 0.05% of the population.

Based on the Canadian population in 2019, 0.05% of the population was 17,350 people. The only “rare” subclass above is the number of Graves’ Disease patients who would test positive on a TBAb-specific assay, which would be estimated at 9,182 Canadians, shown in Table 3.

Percentages of the AITD-TRAb population

Next, let’s look at the percentages of these subclasses in relationship to each other.

Each grand total per country represents the “Autoimmune thyroid disease patients with TRAb antibodies” – which I’ll abbreviate “the AITD-TRAb population.”

Within this AITD-TRAb patient population, only 48.9% will routinely get their antibodies tested in diagnosis: These are the Graves’ Disease hyperthyroid patients who are tested for the TSH-Receptor stimulating antibody, TSAb.

The remainder of AITD-TRAb patients, 51.1%, will have their antibodies ignored.

48.7 % of the AITD-TRAB population are Hashimoto’s patients who won’t likely get tested

24.5% of the AITD-TRAb population are Hashimoto’s patients with TSAb stimulating antibodies

24.2% of the AITD-TRAb population are Hashimoto’s patients with TBAb blocking antibodies.

As for the number of people with each TRAb antibody subtype, roughly 3 out of 4 will have the stimulating variety, and 1 out of 4 the blocking variety:

the TBAb blocking antibody is found in 26.5% of people in the AITD-TRAb population (almost all of them Hashimoto’s)

the TSAb stimulating antibody expresses in 73.4% of people in the AITD-TRAb population (1/3 of whom are Hashimoto’s patients)

Conclusions

We are currently overlooking half the population thyroid patients with TRAb antibodies.

We are overlooking most of these people with antibodies just because they are TBAb blocking antibodies that cause hypothyroidism

Some TSAb stimulating antibodies we ignore because it’s a widespread belief that they can’t exist in hypothyroid people.

What are the implications?

Millions of neglected diagnoses worldwide translate to millions of people who may have increased suffering, health care costs, and unsolved medical mysteries.

But biochemical hypothyroidism is just one of the many manifestations of these antibodies.

Thyroidectomies and radioiodine ablation don’t remove the antibodies. There is no such thing as an antibody-ectomy.

Some therapies for Graves’ powerfully shift the antibodies and can aid remission, but it is not known if thyroid hormone dosing modulates them. Thyroid hormone dosing is a way we compensate for severe TBAb-caused hypothyroidism, but it can’t fix everything these antibodies can do.

By overlooking the blocking antibody in diagnostic testing, we are not using what Diana et al, 2017 calls “an important tool to identify AITD, mainly in the form of reversible hypothyroidism.”

In other words, we may have an unknown number of cases of TBAb-based hypothyroidism that will, or have already, slipped into remission.

What Diana et al fail to note is the bad news. The TBAb antibody can also cause permanent and severe atrophy of the thyroid gland, since these are the antibodies responsible for Atrophic Thyroiditis at any age. TBAb can make untreated hypothyroidism more dangerous, and its onset can be swift.

For some patients, TBAb-TSAb fluctuations are a tug-of-war that makes therapy very complicated and unpredictable: it can force them to cycle through phases of hyper, hypo and euthyroidism over months or years.

In addition, the antibody can cause tissue manifestations beyond the thyroid gland. Just as the Graves’ stimulating antibody activity manifests in eyes, skin, bones, thymus, even when fully euthyroid, the blocking one can as well. All tissues that express TSH receptors may interact with this antibody.

As for the cost of ignorance paid by medical research, consider all the ways in which thyroid therapy clinical trials can be compromised by these antibodies flaring up.

Consider the lack of clarity that will persist about relationships between thyroid autoimmunity and other health conditions. You can’t generalize about “autoimmune hypothyroidism” if 20% of people in this category are distinctly different from their peers in autoimmune etiology and prognosis.